title: Peroxiredoxin 3 is resistant to oxidation-induced apoptosis of Hep-3b cells.
abstract: OBJECTIVE
  Although peroxiredoxin 3 (PRX3) was reported to be overexpressed in liver cancer, the precise function of PRX3 in the development and/or progression of liver cancer remained to be obscure. The present study was conducted to investigate the response of PRX3 to oxidative stress in hepatocellular carcinoma (HCC) cells.
  
  
  METHODS
  After successful knockdown of PRX3 expression by small interfering RNA, we treated HCC cell lines Hep-3b and Hep-G2 with gradient concentrations of H2O2 and detected cell proliferation, apoptosis, and the level of reactive oxygen species (ROS) in the cells.
  
  
  RESULTS
  After low-dose (5-20 μmol/l) H2O2 treatment, the ROS level was significantly higher in PRX3-knockdown Hep-3b cells than in controls. In addition, PRX3 down-regulation resulted in decreased proliferation, increased apoptosis, and increased caspase 3 activity of Hep-3b cells. We did not notice significant difference between PrxIII knockdown and control Hep-G2 cells in ROS level, cell viability or apoptosis.
  
  
  CONCLUSIONS
  Our results suggest that PRX3 is an indispensable ROS scavenger that protects tumor cells against oxidative damage and subsequent apoptosis, which provides a clue that PRX3 may be involved in the chemotherapeutic resistance of liver cancer. The underlying mechanism for PRX3 function needs further investigation.
authors.affiliation: Department of Gastroenterology, Shandong Qianfoshan Hospital, Shandong University, Jinan, 250014, China.
authors.forename: Y-G
authors.initials: YG
authors.lastname: Wang
authors.forename: L
authors.initials: L
authors.lastname: Li
authors.forename: C-H
authors.initials: CH
authors.lastname: Liu
authors.forename: S
authors.initials: S
authors.lastname: Hong
authors.forename: M-J
authors.initials: MJ
authors.lastname: Zhang
mesh_terms: D017209:Apoptosis / Q000187:drug effects*; D015153:Blotting, Western; D006528:Carcinoma, Hepatocellular / Q000378:metabolism / Q000473:pathology*; D053148:Caspase 3 / Q000378:metabolism; D049109:Cell Proliferation / Q000187:drug effects*; D005434:Flow Cytometry; D006801:Humans; D006861:Hydrogen Peroxide / Q000494:pharmacology*; D008113:Liver Neoplasms / Q000378:metabolism / Q000473:pathology*; D016877:Oxidants / Q000494:pharmacology; D010084:Oxidation-Reduction; D061105:Peroxiredoxin III / Q000037:antagonists & inhibitors / Q000235:genetics / Q000378:metabolism*; D034741:RNA, Small Interfering / Q000235:genetics; D017382:Reactive Oxygen Species / Q000378:metabolism*; D014407:Tumor Cells, Cultured
chemical_list: D016877:Oxidants; D034741:RNA, Small Interfering; D017382:Reactive Oxygen Species; D006861:Hydrogen Peroxide; C516115:PRDX3 protein, human; D061105:Peroxiredoxin III; D053148:Caspase 3